A purified fraction of polysaccharides obtained from the fruits of Lycium barbarum L. shaped the gut community profile and improved glucose homeostasis as well as intestinal barrier function in high-fat diet-induced diabetic mice.

The high-fat and high-fructose diet (HFFD) is a common diet in westernized societies, which worsens disturbances in gut microbiota and bile acid (BA) metabolism. Herein, the present study aimed to investigate the effects of the water extract of Lycium barbarum fruits (LBE) on gut microbiota and BA metabolism in mice with HFFD-induced neuroinflammation. The results showed that supplementation of LBE for 14 weeks remarkably ameliorated weight gain and insulin resistance and suppressed microglial activation and neural neuroinflammation induced by HFFD. The results of Morris water maze and Y-maze tests demonstrated that LBE attenuated HFFD-induced cognitive impairment. Moreover, LBE elevated hepatic BA biosynthesis and excretion of BAs and increased elimination of BAs via the feces. Notably, LBE supplementation resulted in the enrichment of tauroursodeoxycholic acid in the cortex and hippocampus. Furthermore, the 16S rDNA sequencing results showed that LBE could modulate the structure of gut microbiota, and in the meantime decrease the relative abundance of Clostridium_XlVa, which is associated with BA homeostasis. Additionally, LBE exerted neuroprotective effects involving the increment of Lactococcus, known as a potentially beneficial bacterium. These results demonstrated that LBE could ameliorate neuroinflammation and cognitive impairment in HFFD-induced mice through the gut–liver–brain axis, which might be due to the regulation of BA homeostasis and gut microbiota in mice.

The aqueous extract of Lycium ruthenicum Murray (LRE) could attenuate neuroinflammation in mice induced by a high-fat and high-fructose diet (HFFD). Moreover, LRE could adjust bile acid (BA) metabolism and the gut microbiota. Behavioral tests revealed that LRE prevented HFFD-induced cognitive deficits. The treatment of LRE resulted in a decreased expression of inflammation-related mRNA of TNF-α, IL-6, and IL-1β in the cerebral cortex and hippocampus. Furthermore, LRE ameliorated gut microbiota disorder caused by HFFD by markedly elevating the relative abundances of Streptococcus and probiotics such as Lactococcus. Concurrently, it reduced the relative abundances of Helicobacter and Clostridium_XIVa. The levels of tauroursodeoxycholic acid, known for its neuroprotective property, and taurocholic acid, recognized as an anti-inflammatory agent, were significantly enhanced in the hippocampus and cerebral cortex due to the treatment with LRE. In a word, LRE might have the potential to alleviate HFFD-induced cognitive dysfunction by modulating intestinal microbiota and promoting the synthesis of neuroprotective BAs.